Listeria monocytogenes PrsA2 is required for virulence factor secretion and bacterial viability within the host cell

Francis Alonzo1, Nancy E Freitag

  • 1Department of Microbiology and Immunology, University of Illinois at Chicago, Chicago, IL 60612-7344, USA.

Infection and Immunity
|September 9, 2010
PubMed

Insights

The bacterial chaperone PrsA2 is crucial for Listeria monocytogenes survival within host cells, aiding virulence factor secretion. PrsA1 does not provide functional overlap, highlighting PrsA2's specific role in pathogenesis.

Area of Science:

  • Microbiology
  • Bacterial Pathogenesis
  • Host-Pathogen Interactions

Background:

  • Facultative intracellular bacteria like Listeria monocytogenes require precise regulation of virulence factors for host cell invasion.
  • Post-translocation secretion chaperones, such as PrsA1 and PrsA2 in L. monocytogenes, are implicated in protein folding and secretion at the bacterial membrane-cell wall interface.
  • PrsA2 is suggested to be specifically adapted for bacterial pathogenesis.

Purpose of the Study:

  • To investigate the roles of PrsA1 and PrsA2 in Listeria monocytogenes growth and protein secretion.
  • To determine the necessity of PrsA2 for bacterial viability within host cell cytosol.
  • To elucidate the functional relationship between PrsA1 and PrsA2.

Main Methods:

  • In vitro and in vivo growth assays for L. monocytogenes strains lacking PrsA1 or PrsA2.
  • Proteomic analysis of prsA2 mutant strains under conditions of activated virulence regulator PrfA.
  • Comparison of amino acid sequences and functional overlap between PrsA1 and PrsA2.

Main Results:

  • Neither PrsA1 nor PrsA2 was essential for L. monocytogenes growth in broth culture.
  • Optimal bacterial viability within host cell cytosol was dependent on PrsA2.
  • PrsA2 activity was critically required under conditions of PrfA activation, mimicking host cell infection.
  • No functional overlap was detected between PrsA2 and PrsA1 despite high sequence similarity.

Conclusions:

  • PrsA2 plays a critical role in Listeria monocytogenes pathogenesis, particularly within the host cell cytosol.
  • PrsA2 is essential for bacterial viability and virulence factor regulation during host cell infection.
  • PrsA1 and PrsA2 are functionally distinct, with PrsA2 uniquely adapted for infection-related processes.

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